Impact of Aging on the Morphology of the Adrenal Gland in Rats / Impacto del Envejecimiento en la Morfología de la Glándula Suprarrenal en Ratas

SUMMARY: Aging is an inevitable biological process that affects the function of all organs, including the adrenal gland, which is essential for producing steroid hormones that regulate metabolism, stress response, and immune activation. Understanding how aging affects the morphology of this gland is crucial to developing interventions to mitigate its adverse effects. Thus, this study aimed to describe the morphoquantitative alterations of the adrenal gland in senescent Sprague Dawley rats compared to adult rats. Twelve male rats were divided into 6 adult rats aged 6 months (group A) and 6 senescent rats aged 36 months (group S). Histopathological studies, quantification of collagen fibers types I and III, and stereological analysis were performed to determine the volume density (Vv), surface area (Sv), and number (Nv) of the nuclei of the zona fasciculata cells. Adrenal gland tissue from group S presented dysplasia, metaplasia, intracellular fat accumulation, fibrosis, blood vessel dilation, and increased presence of apoptotic cells. Capsule thickening and increased collagen type I were also observed. There was a significant decrease in Vv, Sv, and Nv of zona fasciculata nuclei in group S compared to group A. The results indicate that aging induces significant morphoquantitative changes in the adrenal gland, which could contribute to the decrease in glucocorticoid production and alterations in aldosterone and cortisol secretion observed in senescence. Understanding these alterations is crucial to developing interventions that mitigate the adverse effects of aging on the endocrine system.

El envejecimiento es un proceso biológico inevitable que afecta la función de todos los órganos, incluida la glándula suprarrenal, fundamental para la producción de hormonas esteroides que regulan el metabolismo, la respuesta al estrés y la activación inmunológica. Comprender cómo el envejecimiento afecta la morfología de esta glándula es crucial para desarrollar intervenciones que mitiguen sus efectos adversos. Así, el objetivo de este estudio fue describir las alteraciones morfocuantitativas de la glándula suprarrenal en ratas Sprague Dawley senescentes comparadas con ratas adultas. Se utilizaron 12 ratas macho, divididas en dos grupos: 6 ratas adultas de 6 meses de edad (grupo A) y 6 ratas senescentes de 36 meses de edad (grupo S). Se realizaron estudios histopatológicos, cuantificación de fibras de colágeno tipos I y III y análisis estereológicos para determinar la densidad de volumen (Vv), de superficie (Sv) y de número (Nv) de los núcleos de las células de la zona fasciculada. El tejido de la glándula suprarrenal del grupo S presentó displasia, metaplasia, acumulación de grasa intracelular, fibrosis, dilatación de vasos sanguíneos y mayor presencia de células apoptósicas. También se observó un engrosamiento de la cápsula y un incremento del colágeno tipo I. Hubo una disminución significativa en Vv, Sv y Nv de los núcleos de la zona fasciculada en el grupo S en comparación con el grupo A. Los resultados indican que el envejecimiento induce cambios morfocuantitativos significativos en la glándula suprarrenal, lo que podría contribuir a la disminución en la producción de glucocorticoides y alteraciones en la secreción de aldosterona y cortisol observadas en la senescencia. Comprender estas alteraciones es crucial para desarrollar intervenciones que mitiguen los efectos adversos del envejecimiento en el sistema endocrino.

Chemical characterization and effects of volatile oil of Alpinia zerumbet on the quality of collagen deposition and caveolin-1 expression in a muscular fibrosis murine model / Caracterização química e efeitos do óleo volátil de Alpinia zerumbet na qualidade da deposição do colágeno e expressão da caveolina-1 em modelo murino de fibrose muscular

Abstract This study evaluated the effect of the volatile oil of Alpinia zerumbet (VOAz) on caveolin-1 gene expression and muscular fibrosis. The rats were immobilized to induce fibrosis of the gastrocnemius muscle, and they were treated with VOAz. Collagen quality was assessed by histology and the expression of the caveolin-1 (CAV-1) gene was evaluated using qPCR. Histomorphological analysis indicated a significant reduction in the perimeter, width, and intensity of collagen in the treated groups, thus showing that the oil was effective in regulating the quality of collagen at the three concentrations. The results of expression levels suggested a decrease in the lesioned group and in two treatment groups (0.0115 µg/g and 0.009 µg/g). However, with the lowest concentration (0.0065 µg/g), no significant difference was observed, with levels similar to those found in healthy tissue. Therefore, the results showed that VOAz has the potential to be a non-invasive and low-cost alternative to aid in the treatment of muscular fibrosis.

Resumo Este estudo avaliou o efeito do óleo volátil de Alpinia zerumbet (OVAz) na expressão do gene da caveolina-1 e na fibrose muscular. Os ratos foram imobilizados para induzir a fibrose do músculo gastrocnêmio, e foram tratados com OVAz. A qualidade do colágeno foi avaliada com histologia e à expressão do gene caveolina-1 (CAV-1) foi avaliada usando qPCR. A análise histomorfológica indicou uma redução significativa no perímetro, largura e intensidade do colágeno nos grupos tratados. Os resultados dos níveis de expressão sugeriram diminuição nos grupos de lesão e em dois grupos de tratamento (0,0115 µg/g e 0,009 µg/g). No entanto, com a menor concentração (0,0065 µg/g), não foi observada diferença significativa, apresentando níveis semelhantes aos encontrados em tecido saudável. O uso do OVAz foi eficaz para reverter as alterações do colágeno causadas pela fibrose, e sua menor concentração apresentou uma possível tendência de aumento na expressão do CAV-1. Portanto, os resultados mostraram que o OVAz tem potencial para ser uma alternativa não invasiva e de baixo custo para auxiliar no tratamento da fibrose muscular.

Therapeutic potential of stem cell and melatonin on the reduction of CCl4-induced liver fibrosis in experimental mice model / Potencial terapêutico de células-tronco e melatonina na redução da fibrose hepática induzida por CCl4 no modelo de ratos experimentais

Liver fibrosis is initial stage of any chronic liver disease and its end stage is develops into cirrhosis. Chronic liver diseases are a crucial global health issue and the cause of approximately 2 million deaths per year worldwide. Cirrhosis is currently the 11th most common cause of death globally. Mesenchymal stem cell (MSCs) treatment is the best way to treat acute and chronic liver disease. The aim of this study is to improve the therapeutic potential of MSCs combined with melatonin (MLT) to overcome CCl4-induced liver fibrosis and also investigate the individual impact of melatonin and MSCs against CCl4-induced liver impairment in animal model. Female BALB/c mice were used as CCL4-induced liver fibrotic animal model. Five groups of animal model were made; negative control, Positive control, CCl4+MSCs treated group, CCl4+MLT treated group and CCl4+MSCs+MLT treated group. Cultured MSCs from mice bone marrow were transplanted to CCl4-induced liver injured mice model, individually as well as together with melatonin. Two weeks after MSCs and MLT administration, all groups of mice were sacrificed for examination. Morphological and Histopathological results showed that combined therapy of MSCs+MLT showed substantial beneficial impact on CCl4-induced liver injured model, compared with MSCs and MLT individually. Biochemically, considerable reduction was observed in serum bilirubin and ALT levels of MLT+MSC treated mice, compared to other groups. PCR results shown down-regulation of Bax and up-regulation of Bcl-xl and Albumin, confirm a significant therapeutic effect of MSCs+MLT on CCI4-induced liver fibrosis. From the results, it is concluded that combined therapy of MSCs and MLT show strong therapeutic effect on CCL4-induced liver fibrosis, compared with MSCs and MLT individually.

A fibrose hepática é a fase inicial de qualquer doença hepática crônica, e em sua fase final desenvolve-se para cirrose. As doenças hepáticas crônicas são uma questão de saúde global crucial e a causa de aproximadamente 2 milhões de mortes por ano em todo o mundo. A cirrose, hoje em dia, é a 11ª causa mais comum de morte globalmente. O tratamento da célula-tronco mesenquimal (MSCs) é uma maneira eletiva de tratar a doença hepática aguda e crônica. O objetivo deste estudo é melhorar o potencial terapêutico dos MSCs combinados com a melatonina (MLT) para superar a fibrose hepática induzida por CCl4 e também investigar o impacto individual da melatonina e MSCs contra o comprometimento do fígado induzido por CCl4 no modelo animal. Os ratos BALB / C fêmeas foram usados ​​como modelo de animal fibrótico de fígado induzido por CCl4. Cinco grupos de modelo animal foram feitos: Controle Negativo, Controle Positivo, CCl4 + MSCs Tratados Grupo, Grupo Tratado CCl4 + MLT e Grupo Tratado CCl4 + MSCs + MLT. MSCs cultivados da medula óssea dos ratos foram transplantados para o modelo de camundongos de fígado induzido por CCl4, individualmente, bem como em conjunto com a melatonina. Duas semanas após a administração MSCs e MLT, todos os grupos de camundongos foram sacrificados para o exame. Os resultados morfológicos e histopatológicos mostraram que a terapia combinada do MSCs + MLT mostrou impacto benéfico substancial no modelo ferido no fígado induzido pelo CCl4, em comparação com o MSCs e o MLT individualmente. A redução bioquimicamente considerável foi observada em bilirrubina sérica e níveis ALT de ratinhos tratados com MLT + MSCs, em comparação com outros grupos. Os resultados de PCR mostraram regulação negativa do BAX e regulação positiva do BCL-XL e da albumina, confirmando um efeito terapêutico significativo do MSCs + MLT na fibrose hepática induzida por CCl4. Dos resultados, conclui-se que a terapia combinada de MSCs e MLT mostram um forte efeito terapêutico na fibrose hepática induzida por CCl4, em comparação com MSCs e MLT individualmente.

Endometrial mesenchymal stromal/stem cells improve regeneration of injured endometrium in mice

BACKGROUND: The monthly regeneration of human endometrial tissue is maintained by the presence of human endometrial mesenchymal stromal/stem cells (eMSC), a cell population co-expressing the perivascular markers CD140b and CD146. Endometrial regeneration is impaired in the presence of intrauterine adhesions, leading to infertility, recurrent pregnancy loss and placental abnormalities. Several types of somatic stem cells have been used to repair the damaged endometrium in animal models, reporting successful pregnancy. However, the ability of endometrial stem cells to repair the damaged endometrium remains unknown. METHODS: Electrocoagulation was applied to the left uterine horn of NOD/SCID mice causing endometrial injury. Human eMSC or PBS was then injected into the left injured horn while the right normal horn served as controls. Mice were sacrificed at different timepoints (Day 3, 7 and 14) and the endometrial morphological changes as well as the degree of endometrial injury and repair were observed by histological staining. Gene expression of various inflammatory markers was assessed using qPCR. The functionality of the repaired endometrium was evaluated by fertility test. RESULTS: Human eMSC successfully incorporated into the injured uterine horn, which displayed significant morphological restoration. Also, endometrium in the eMSC group showed better cell proliferation and glands formation than the PBS group. Although the number of blood vessels were similar between the two groups, gene expression of VEGF-α significantly increased in the eMSC group. Moreover, eMSC had a positive impact on the regeneration of both stromal and epithelial components of the mouse endometrium, indicated by significantly higher vimentin and CK19 protein expression. Reduced endometrial fibrosis and down-regulation of fibrosis markers were also observed in the eMSC group. The eMSC group had a significantly higher gene expression of anti-inflammatory factor Il-10 and lower mRNA level of pro-inflammatory factors Ifng and Il-2, indicating the role of eMSC in regulation of inflammatory reactions. The eMSC group showed higher implantation sites than the PBS group, suggesting better endometrial receptivity with the presence of newly emerged endometrial lining. CONCLUSIONS: Our findings suggest eMSC improves regeneration of injured endometrium in mice.

Captopril inhibits thioacetamide-induced chronic liver injury associated with the suppression of inflammation / hypoxia- inducible factor 1-alpha / profibrogenic axis-mediated hepatotoxicity in rats / Captopril inhibe la lesión hepática crónica inducida por tioacetamida asociada con la supresión de la inflamación/factor 1-alfa inducible por hipoxia/hepatotoxicidad mediada por el eje profibrogénico en rata

SUMMARY: Liver transplantation is the only available method to treat liver failure induced by chronic liver injury. We sought to determine whether the angiotensin-converting enzyme inhibitor, captopril, can inhibit the development of chronic liver injury induced by the hepatotoxic agent thioacetamide (TAA) in association with the suppression of inflammation (hsCRP, TNF-α, and IL-6) / hypoxia- inducible factor 1-alpha (HIF-1α) / profibrosis (TIMP-1, MMP-9, and α-SMA) axis that mediates liver injury. Therefore, the model group of rats was injected for eight weeks with 200 mg/kg TAA starting at week two. The protective group was pretreated with 150 mg/ kg captopril daily for two weeks prior to TAA injections and continued receiving both capropril and TAA agents until being humanely scrificed at week 10. We observed a substantial damage to liver tissue in the model group as demonstrated by a significant (p<0.0001) increase in blood and hepatic tissue levels of high sensitivity C-reactive protein (hsCRP), tumor necrosis factor-a (TNF-α), interleukin- 6 (L-6), HIF-1α, tissue inhibitor of metalloproteinases-1 (TIMP-1), matrix metalloproteinase-9 (MMP-9), alpha-smooth muscle actin (α-SMA), alanine aminotransferase (ALT), and aspartate aminotransferase (AST). All these parameters were significantly (p<0.0244) protected by captopril. Also, a significant (p<0.0001) positive correlation was observed between a-SMA (profibrosis) and the serum and tissue levels of hsCRP, TNF-α, HIF-1α, TIMP-1, MMP-9, and ALT. Thus, these findings suggest that the induction of chronic liver injury by the hepatotoxic compound, TAA is associated with the upregulation of inflammation/HIF-1α/profibrosis, with captopril exhibiting beneficial hepatic pleotropic effects.

El trasplante de hígado es el único método disponible para tratar la insuficiencia hepática inducida por una lesión hepática crónica. Buscamos determinar si el inhibidor de la enzima convertidora de angiotensina, captopril, puede inhibir el desarrollo de lesión hepática crónica inducida por el agente hepatotóxico tioacetamida (TAA) en asociación con la supresión de la inflamación (hsCRP, TNF-α e IL-6) / factor inducible por hipoxia 1-alfa (HIF-1α) / profibrosis (TIMP-1, MMP-9 y α- SMA) eje que media la lesión hepática. Por lo tanto, al grupo modelo de ratas se le inyectó durante ocho semanas 200 mg/kg de TAA a partir de la semana dos. El grupo protector fue pretratado con 150 mg/kg de captopril al día durante dos semanas antes de las inyecciones de TAA y continuó recibiendo capropril y agentes TAA hasta que fue sacrificado en la semana 10. Observamos un daño sustancial en el tejido hepático en el grupo modelo, como lo demuestra un aumento significativo (p<0,0001) de los niveles en sangre y tejido hepático de proteína C reactiva de alta sensibilidad (hsCRP), factor de necrosis tumoral-α (TNF-a), interleucina-6 (L-6), HIF-1α, inhibidor tisular de metaloproteinasas-1 (TIMP-1), metaloproteinasa de matriz-9 (MMP-9), actina de músculo liso alfa (α-SMA), alanina aminotransferasa (ALT) y aspartato aminotransferasa (AST). Todos estos parámetros estaban significativamente (p<0,0244) protegidos por captopril. Además, se observó una correlación positiva significativa (p<0,0001) entre α-SMA (profibrosis) y los niveles séricos y tisulares de hsCRP, TNF-α, HIF-1α, TIMP- 1, MMP-9 y ALT. Por lo tanto, estos hallazgos sugieren que la inducción de daño hepático crónico por el compuesto hepatotóxico, TAA, está asociada con la regulación al alza de la inflamación/HIF-1α/profibrosis, con captopril exhibiendo efectos pleotrópicos hepáticos beneficiosos.

A rat model of rheumatoid arthritis: TDZD-8 is associated with the protection against the induction of the synovium knee joint IL-17A/GSK3beta/ROS/alpha-SMA axis of fibrosis / Un modelo de rata de artritis reumatoide: TDZD-8 está asociado con la protección contra la inducción del eje de fibrosis de la articulación sinovial de la rodilla IL-17A/GSK3ß/ROS/α-SMA

SUMMARY: Rheumatoid arthritis (RA) that affects the synovial knee joint causes swelling of the synovial membrane and tissue damage. Interleukin-17A (IL-17A) and the enzyme glycogen synthase kinase-3β (GSK3β) are involved in the pathogenesis of RA. The link between IL-17A, GSK3β, the oxidative stress, and the profibrogenic marker alpha-smooth muscle actin (α-SMA) with and without TDZD-8, GSK3β inhibitor has not been studied before. Consequently, active immunization of rats was performed to induce RA after three weeks using collagen type II (COII) injections. The treated group received daily injection of 1 mg/kg TDZD-8 for 21 days following the immunization protocol (COII+TDZD-8). Blood and synovium tissue samples were harvested at the end of the experiment. RA development was confirmed as corroborated by a substantial increase in blood levels of the highly specific autoantibody for RA, anti-citrullinated protein antibody as well as augmentation of reactive oxidative species (ROS) levels measured as lipid peroxidation. RA induction also increased synovium tissue levels of IL-17A and the profibrogenic marker, α-SMA. All these parameters seemed to be significantly (p<0.0001) ameliorated by TDZD-8. Additionally, a significant correlation between IL-17A, ROS, and α-SMA and biomarkers of RA was observed. Thus, knee joint synovium RA induction augmented IL-17A/GSK3β/ROS/α-SMA axis mediated arthritis in a rat model of RA, which was inhibited by TDZD-8.

La artritis reumatoide (AR) que afecta la articulación sinovial de la rodilla provoca inflamación de la membrana sinovial y daño tisular. La interleucina-17A (IL-17A) y la enzima glucógeno sintasa quinasa-3β (GSK3β) están involucradas en la patogenia de la AR. No se ha estudiadol vínculo entre IL-17A, GSK3β, el estrés oxidativo y el marcador profibrogénico actina de músculo liso alfa (α-SMA) con y sin inhibidor de TDZD-8, GSK3β. En consecuencia, se realizó una inmunización activa de ratas para inducir la AR después de tres semanas usando inyecciones de colágeno tipo II (COII). El grupo tratado recibió una inyección diaria de 1 µg/ kg de TDZD-8 durante 21 días siguiendo el protocolo de inmunización (COII+TDZD-8). Se recogieron muestras de sangre y tejido sinovial al final del experimento. El desarrollo de AR se confirmó como lo corroboró el aumento sustancial en los niveles sanguíneos del autoanticuerpo altamente específico para AR, el anticuerpo antiproteína citrulinada, así como el aumento de los niveles de especies oxidativas reactivas (ROS) medidos como peroxidación lipídica. La inducción de AR también aumentó los niveles de tejido sinovial de IL-17A y el marcador profibrogénico, α-SMA. Todos estos parámetros parecían mejorar significativamente (p<0,0001) con TDZD-8. Además, se observó una correlación significativa entre IL- 17A, ROS y α-SMA y biomarcadores de AR. Por lo tanto, la inducción de AR en la sinovial de la articulación de la rodilla aumentó la artritis mediada por el eje IL-17A/GSK3β/ROS/α-SMA en un modelo de rata de AR, que fue inhibida por TDZD-8.

Rinofima: reporte de un caso de Clínica Estrella / Rhinophyma: a case report of Clínica Estrella

La rinofima es una patología que se caracteriza por presentar hipertrofia de las glándulas sebáceas con proliferación de tejido fibroso, donde la nariz toma un aspecto lobulado dando como resultado la deformidad de la punta nasal; es una forma de rosácea. La prevalencia de esta variedad de rosácea es de aproximadamente un 5-7% en la población y con predominio en el sexo masculino de la quinta a séptima década de vida. Su etiología no se conoce con exactitud. Se presenta el caso de un paciente masculino de 84 años, con antecedentes patológicos de hipertensión arterial e hipotiroidismo; su lesión inició hace 10 años, como una lesión eritematosa con presencia de telangiectasia a nivel de alas y punta nasal, no dolorosa. Se realizó tratamiento con bisturí frío y radiofrecuencia, se realizaron cortes transversales hasta dejar el lecho desprovisto del tumor y finalmente se usó radiofrecuencia en toda la superficie de la lesión restante. Se realizó el procedimiento ambulatorio sin complicaciones inmediatas o tardías

Rhinophyma is a pathology characterized by hypertrophy of the sebaceous glands with proliferation of fibrous tissue, the nose has a lobed appearance, as a result there is a deformity of the nasal tip; rhinophyma is a form of rosacea. The prevalence of this variety of rosacea is approximately 5-7% in the population and predominantly in males from the fifth to seventh decade of life, the etiology is not well known, however there are several predisposing genetic and environmental factors. We present the case of an 84-year-old male patient with a pathological history of arterial hypertension and hypothyroidism; his lesion began 10 years ago, as an erythematous lesion with presence of telangiectasia in the wings and nasal tip, not painful. Treatment was performed with a cold scalpel and radiofrequency, transverse cuts were made until the tumor was gone, and finally radiofrequency was used on the entire surface of the remaining lesion. The outpatient procedure was performed without immediate or late complications.

Variaciones morfológicas de la glándula submandibular en ratas obesas por acción de glutamato monosódico / Morphological variations of the submandibular gland in obese rats by the action of monosodium glutamate

Este estudio tuvo como objetivo demostrar la existencia de variaciones morfológicas en el tejido conectivo de la glándula submandibular de ratas obesas expuestas a glutamato monosódico (GMS). Se utilizaron 12 ratas Sprague Dawley machos recién nacidas (6 ratas para el grupo 1, control; 6 ratas para el grupo 2 (GMS), 4 mg/g de glutamato monosódico de peso (5 dosis) mantenidas por 16 semanas respectivamente con una dieta y agua ad libitum. En el estudio se realizó un análisis estereológico e histológico, demostrándose una variación en el tejido conectivo presentando una disminución del volúmen glandular, mayor fibrosis, y disminución de adipocitos a nivel periférico siendo reemplazado por tejido rico en colágeno. Los vasos sanguíneos observados a nivel estereológico no presentan mayores cambios en cuanto a volumen, superficie y área.

SUMMARY: This study aims to demonstrate the existence of morphological variations in the connective tissue of the submandibular gland of obese rats exposed to MSG. Twelve male newborn Sprague Dawley rats were used (6 rats for group 1, control; 6 rats for group 2 (MSG), 4 mg/g of monosodium glutamate of weight (5 doses) maintained for 16 weeks respectively with a diet and water ad libitum. In the study, a stereological and histological analysis was carried out, demonstrating a variation in the connective tissue, presenting a decrease in the glandular volume, greater fibrosis, and a decrease in adipocytes at the peripheral level, being replaced by tissue rich in collagen. Blood cells observed at the stereological level do not present major changes in terms of volume, surface and area, but in the histological study greater vascularization is observed.

Producción científica en investigación sobre avances terapéuticos de la Enfermedad de Peyronie durante los últimos 62 años. Un análisis bibliométrico / Scientific production on research on therapeutic advances in Peyronie's Disease during the last 62 Years. A bibliometric analysis / Produção científica em pesquisa sobre avanços terapêuticos na Doença de Peyronie nos últimos 62 anos. Uma análise bibliométrica

Introducción. La enfermedad de Peyronie es una malformación adquirida del pene, originada por la deposición de placas fibróticas en la túnica albugínea. La prevalencia en Estados Unidos oscila entre el 0.39% y 11.8%, en Europa 8.9%, en Latinoamérica no existe un porcentaje puntual de prevalencia actual debido a la escasez de reportes de esta patología. Este análisis bibliométrico busca describir la evolución terapéutica de la Enfermedad de Peyronie en la literatura de los últimos 62 años, así como la distribución geográfica de estas publicaciones. Metodología. Estudio observacional, descriptivo, un análisis bibliométrico desde 1957 hasta 2019, utilizando GoPubMed y FABUMED. Resultados. Se obtuvieron 721 referencias sobre tratamiento quirúrgico en enfermedad de Peyronie, con un aumento de la producción científica a lo largo del periodo de estudio. The Journal of Urology fue la revista con mayor cantidad de publicaciones, el 57.9% dentro de la categoría de artículo científico. El país líder fue Estados Unidos con 191 publicaciones. Discusión. Existe poca literatura sobre los avances terapéuticos para el tratamiento de enfermedad de Peyronie, lo que dificulta la comparación de las investigaciones a lo largo de los años en diferentes zonas del mundo. La investigación en Latinoamérica es escasa. Conclusión. La investigación sobre el tratamiento quirúrgico en enfermedad de Peyronie muestra un patrón ascendente en la productividad científica durante los años estudiados. Los países con mayores ingresos económicos son de mayor desarrollo en el tema y en menor medida regiones con recursos limitados. El análisis evidencia la importancia de aumentar producción científica en Colombia, así como estimular la investigación sobre este tema, ya que existen muy pocas publicaciones sobre la evolución del tratamiento quirúrgico para esta enfermedad. Palabras clave: Induración Peniana; Enfermedades del Pene; Bibliometría; Fibrosis; Erección Peniana

Introduction. Peyronie's disease is an acquired malformation of the penis, caused by the deposition of fibrotic plaques in the tunica albuginea. The prevalence in the United States ranges between 0.39% and 11.8%, in Europe 8.9%, in Latin America there is no specific percentage of current prevalence due to the scarcity of reports of this pathology. This bibliometric analysis seeks to describe the therapeutic evolution of Peyronie's Disease in the literature over the last 62 years, as well as the geographic distribution of these publications. Methodology. This is an observational, descriptive study, with a bibliometric analysis from 1957 to 2019, using GoPubMed and FABUMED. Results. 721 references on surgical treatment in Peyronie's disease were obtained, with an increase in scientific production throughout the study period. The Journal of Urology was the journal with the highest number of publications, 57.9% within the scientific article category. The leading country was the United States with 191 publications. Discussion. There is a limited amount of literature on therapeutic advances for the treatment of Peyronie's disease, which makes it difficult to compare research over the years in different areas of the world. Research in Latin America is scarce. Conclusion. Research on surgical treatment in Peyronie's disease shows an increasing pattern in scientific productivity over the years. Countries with higher economic income have greater development in the subject and to a lesser extent regions with limited resources. The analysis shows the importance of increasing scientific production in Colombia, as well as stimulating research on this topic, since there are few publications on the evolution of surgical treatment for this disease. Keywords: Penile Induration; Penile Diseases; Bibliometrics; Fibrosis; Penile Erection

Introdução. A doença de Peyronie é uma malformação adquirida do pênis, causada pela deposição de placas fibróticas na túnica albugínea. A prevalência nos Estados Unidos varia entre 0.39% e 11.8%, na Europa 8.9%, na América Latina não existe um percentual específico de prevalência atual devido à escassez de relatos desta patologia. Esta análise bibliométrica tem como objetivo descrever a evolução terapêutica da Doença de Peyronie na literatura dos últimos 62 anos, bem como a distribuição geográfica destas publicações. Metodologia. Estudo observacional, descritivo, análise bibliométrica de 1957 a 2019, utilizando GoPubMed e FABUMED. Resultados. Foram obtidas 721 referências sobre tratamento cirúrgico na doença de Peyronie, com aumento da produção científica ao longo do período do estudo. The Journal of Urology foi o periódico com maior número de publicações, 57.9% dentro da categoria artigo científico. O país líder foram os Estados Unidos com 191 publicações. Discussão. Há pouca literatura sobre avanços terapêuticos para o tratamento da doença de Peyronie, o que dificulta a comparação de pesquisas ao longo dos anos em diferentes partes do mundo. As pesquisas na América Latina são escassas. Conclusão. As pesquisas sobre o tratamento cirúrgico da doença de Peyronie mostram um padrão crescente de produtividade científica ao longo dos anos estudados. Os países com maior rendimento económico são mais desenvolvidos no assunto e, em menor medida, regiões com recursos limitados. A análise mostra a importância de aumentar a produção científica na Colômbia, bem como estimular a pesquisa sobre o tema, uma vez que existem poucas publicações sobre a evolução do tratamento cirúrgico desta doença. Palavras-chave: Induração Peniana; Doenças do Pênis; Bibliometria; Fibrose; Ereção Peniana

Prospective insight into the role of benzyl propylene glycoside as a modulator of the cGAS-STING signaling pathway in the management of nonalcoholic fatty pancreas animal model

BACKGROUND: Nonalcoholic fatty pancreatitis (NAFP) is one of the metabolic syndrome manifestations that need further studies to determine its molecular determinants and find effective medications. We aimed to investigate the potential effect of benzyl propylene glycoside on NAFP management via targeting the pancreatic cGAS-STING pathway-related genes (DDX58, NFκB1 & CHUK) and their upstream regulator miRNA (miR-1976) that were retrieved from bioinformatics analysis. METHODS: The rats were fed either normal chow or a high-fat high-sucrose diet (HFHS), as a nutritional model for NAFP. After 8 weeks, the HFHS-fed rats were subdivided randomly into 4 groups; untreated HFHS group (NAFP model group) and three treated groups which received 3 doses of benzyl propylene glycoside (10, 20, and 30 mg/kg) daily for 4 weeks, parallel with HFHS feeding. RESULTS: The molecular analysis revealed that benzyl propylene glycoside could modulate the expression of the pancreatic cGAS-STING pathway-related through the downregulation of the expression of DDX58, NFκB1, and CHUK mRNAs and upregulation of miR-1976 expression. Moreover, the applied treatment reversed insulin resistance, inflammation, and fibrosis observed in the untreated NAFP group, as evidenced by improved lipid panel, decreased body weight and the serum level of lipase and amylase, reduced protein levels of NFκB1 and caspase-3 with a significant reduction in area % of collagen fibers in the pancreatic sections of treated animals. CONCLUSION: benzyl propylene glycoside showed a potential ability to attenuate NAFP development, inhibit pancreatic inflammation and fibrosis and reduce the pathological and metabolic disturbances monitored in the applied NAFP animal model. The detected effect was correlated with modulation of the expression of pancreatic (DDX58, NFκB1, and CHUK mRNAs and miR-1976) panel.

Alpha-kinase1 promotes tubular injury and interstitial inflammation in diabetic nephropathy by canonical pyroptosis pathway

BACKGROUND: Alpha-kinase 1 (ALPK1) is a master regulator in inflammation and has been proved to promote renal fibrosis by promoting the production of IL-1ß in diabetic nephropathy (DN) mice. Pyroptosis is involved in high glucose (HG)-induced tubular cells injury, characterized by activation of Gasdermin D (GSDMD) and the release of IL-1ß and IL-18, resulting in inflammatory injury in DN. It is reasonable to assume that ALPK1 is involved in pyroptosis-related tubular injury in DN. However, the mechanism remains poorly defined. METHODS: Immunohistochemistry (IHC) staining was performed to detect the expression of pyroptosis- and fibrosis-related proteins in renal sections of DN patients and DN mice. DN models were induced through injection of streptozotocin combined with a high-fat diet. Protein levels of ALPK1, NF-κB, Caspase-1, GSDMD, IL-1ß, IL-18 and α-SMA were detected by Western blot. HK-2 cells treated with high-glucose (HG) served as an in vitro model. ALPK1 small interfering RNA (siRNA) was transfected into HK-2 cells to down-regulate ALPK1. The pyroptosis rates were determined by flow cytometry. The concentrations of IL-1ß and IL-18 were evaluated by ELISA kits. Immunofluorescence staining was used to observe translocation of NF-κB and GSDMD. RESULTS: The heat map of differentially expressed genes showed that ALPK1, Caspase-1 and GSDMD were upregulated in the DN group. The expression levels of ALPK1, Caspase-1, GSDMD and CD68 were increased in renal biopsy tissues of DN patients by IHC. ALPK1expression and CD68+ macrophages were positively correlated with tubular injury in DN patients. Western blot analysis showed increased expressions of ALPK1, phospho-NF-κB P65, GSDMD-NT, and IL-1ß in renal tissues of DN mice and HK-2 cells, accompanied with increased renal fibrosis-related proteins (FN, α-SMA) and macrophages infiltration in interstitial areas. Inhibition of ALPK1 attenuated HG-induced upregulation expressions of NF-κB, pyroptosis-related proteins Caspase-1, GSDMD-NT, IL-1ß, IL-18, α-SMA, and pyroptosis level in HK-2 cells. Also, the intensity and nuclear translocation of NF-κB and membranous translocation of GSDMD were ameliorated in HG-treated HK-2 cells after treatment with ALPK1 siRNA. CONCLUSIONS: Our data suggest that ALPK1/NF-κB pathway initiated canonical caspase-1-GSDMD pyroptosis pathway, resulting in tubular injury and interstitial inflammation of DN.

Experiencia de downstaging versus criterios de Milán para trasplante hepático por carcinoma hepatocelular en una cohorte prospectiva / Experience with downstaging versus Milan criteria for liver transplantation in patients with hepatocellular carcinoma in a prospective cohort

Introducción. El acceso al trasplante hepático (TH) en pacientes con carcinoma hepatocelular (CHC) se basa en la aplicación de criterios morfológicos rigurosos estipulados desde 1996, co-nocidos como criterios de Milán. Una de las estrategias descritas para expandir estos criterios se conoce como downstaging (reducción del estadiaje tumoral mediante terapias locorregionales). El objetivo de este estudio fue describir el comportamiento postrasplante de pacientes con CHC que ingresaron dentro de los parámetros de Milán, comparado con el de aquellos pacientes llevados a terapia de downstaging en un centro colombiano. Metodología. Se incluyeron pacientes adultos con cirrosis hepática (CH) y CHC que fueron llevados a TH en el Hospital Pablo Tobón Uribe, entre julio de 2012 a septiembre de 2021. Como desenlace principal se definió recurrencia y tiempo de recurrencia de la enfermedad tumoral, muerte por todas las causas y tiempo al fallecimiento. Se evaluaron las características sociodemográficas y clínicas de cada grupo. Se incluyeron scores pronósticos de recurrencia de la enfermedad tumoral. Resultados. Se trasplantaron 68 pacientes con CH y CHC, 50 (73,5 %) eran hombres y la edad promedio fue 59 años; 51 pacientes (75 %) cumplían con los criterios de Milán y 17 (25 %) fueron llevados a terapia de downstaging previo al TH. No hubo diferencias significativas en la supervivencia global y supervivencia libre de trasplante entre los dos grupos evaluados, p=0,479 y p=0,385, respectivamente. Tampoco hubo diferencia significativa en la recurrencia de la enfermedad tumoral entre ambos grupos (p=0,81). En total hubo 7 casos de recurrencia tumoral (10,2 %) y 11 casos de muerte (16,2 %). Conclusiones. No se encontraron diferencias significativas en recurrencia y mortalidad entre los pacientes que cumplían los criterios de Milán y los trasplantados luego de la terapia de downstaging, en un tiempo de se-guimiento de 53 meses hasta el último control posterior al trasplante hepático. Esta sería la primera evaluación prospectiva de un protocolo de downstaging para CHC en Colombia.

Introduction. Access to liver transplantation (LT) in patients with hepatocellular carcinoma (HCC) is based on the application of rigorous morphological criteria stipulated since 1996, known as the Milan criteria. One of the strategies described to expand these criteria is known as downstaging (tu-mor staging reduction through locoregional therapies). The objective of this study was to describe the post-transplant performance of patients with HCC who were admitted within the Milan parameters, compared with those of patients taken to downstaging therapy, in a Colombian center. Methodolo-gy. Adult patients with cirrhosis and HCC that received LT between July 2012 and September 2021 at the Pablo Tobón Uribe Hospital were included. The main outcome was defined as recurrence and time to recurrence of the tumor disease, death from all causes, and time to death. The socio-demographic and clinical characteristics of each group were evaluated. Tumor disease recurrence prognostic scores were included. Results. Sixty-eight patients with cirrhosis and HCC received LT in the time frame, 50 (73.5%) were men and the mean age was 59 years. Fifty-one patients were trans-planted (75%) fulfilling Milan criteria, and 17 (25%) patients received downstaging therapies before LT. There were no significant differences in overall survival and transplant-free survival between the two groups, p=0.479 and p=0.385, respectively. There was also no significant difference in the recurrence of the tumor disease between both groups (p=0.81). In total there were 7 tumoral recurrences (10.2%) and 11 deaths (16.2%). Conclusions. There were no differences in recurrence and survival between patients transplanted fulfilling Milan criteria and those receiving downstaging therapies, following a mean time of 53 months after LT. This is the first prospective evaluation of the downstaging protocol in Colombia.

Falla hepática aguda sobre crónica / Acute on chronic liver failure

La falla hepática aguda sobre crónica (ACLF) es un síndrome que se presenta en pacientes con cirrosis descompensada, y se caracteriza por una mortalidad elevada a 28 días, que se diagnostica con la combinación de falla hepática y extrahepática. Se han publicado numerosas definiciones, de las cuales se resalta la realizada por la Asociación Europea para el Estudio del Hígado (EASL), la cual tiene en cuenta 6 sistemas orgánicos (hígado, riñón, pulmón, cerebro, coagulación y circulación), y gradúa su gravedad basada en el número de sistemas comprometidos en el momento de la presentación. Entre los pilares en el abordaje del paciente con ACLF es imperiosa la búsqueda de los factores precipitantes, siendo los más frecuentes las infecciones bacterianas, el consumo excesivo de alcohol, la hemorragia de vías digestivas, la injuria hepática inducida por medicamentos y la cirugía hepática o cirugía mayor, teniendo en cuenta que aproximadamente en el 50 % de los casos no se logrará establecer la causa. Los pilares angulares del tratamiento constarán de la reversión o interrupción del factor precipitante, el soporte orgánico y, en aquellos pacientes que cumplan los criterios para trasplante, su realización oportuna.

Acute-on-chronic liver failure is a syndrome that occurs in patients with acute decompensated cirrhosis and is characterized by high 28-day mortality that is diagnosed with a combination of hepatic and extrahepatic organ failure. Numerous definitions have been published with great concern related to the etiology and cause of the decompensation, of which the one made by the European Association for the Study of the Liver (EASL) stands out, taking into account 6 organic systems (liver, kidney, lung, brain, coagulation, and circulation), and grades its severity based on the number of systems involved at the time of presentation. Among the pillars in the approach to the patient with ACLF, the search for precipitating factors is imperative, the most frequent being bacte-rial infections, excessive alcohol consumption, digestive tract bleeding, drug-induced liver injury, liver surgery or major surgery, keeping in mind that in approximately 50% of cases the cause will not be established. The cornerstones of treatment will consist of the reversal or interruption of the precipitating factor, organ support and, in those patients who meet the criteria for transplantation, its timely performance.

Uso de albúmina a largo plazo en el paciente cirrótico. Revisión sistemática / Long-term use of albumin in the cirrhotic patient. Systematic review

Introducción. La cirrosis constituye la etapa final de la enfermedad hepática crónica, con una alta mortalidad, y puede deberse a diferentes etiologías. La albúmina tiene tres indicaciones bien establecidas: la prevención de la disfunción circulatoria inducida por paracentesis, la peritonitis bacteriana espontánea y el síndrome hepatorrenal, sin embargo, su uso a largo plazo es controvertido. El objetivo de esta revisión fue identificar si el uso prolongado de la albúmina tiene efectos beneficiosos en el tratamiento de pacientes cirróticos. Metodología. Se realizaron búsquedas en la base de datos de PubMed, empleando los siguientes términos: ("Liver Cirrhosis"[Mesh]) AND ("Serum Albumin"[Mesh] OR "Serum Albumin, Human"[Mesh]). Se excluyeron los artículos que no cumplieron con la temática y aquellos que tenían más de 5 años de antigüedad, a excepción de aquellos relevantes para la revisión. Resultados. Se ha demos-trado en varios estudios realizados en los últimos 4 años, que la administración prolongada de albúmina reduce la mortalidad en el paciente cirrótico. Además, resulta en una disminución en ingresos hospitalarios por complicaciones de la cirrosis, disminución de la necesidad de para-centesis y menor uso de albúmina para otras indicaciones ya establecidas, lo que contrarresta los costos derivados de la terapia. Conclusión. Se concluye con base en la evidencia presenta-da, que el uso de albúmina a largo plazo podría resultar beneficioso en pacientes con cirrosis hepática descompensada. No obstante, es necesario abordar otros aspectos de la terapia en estudios posteriores

Introduction. Cirrhosis is the final stage of chronic liver disease, has a high mortality and can be due to different etiologies. Albumin has three well-established indications: prevention of circulatorydysfunction induced by paracentesis, spontaneous bacterial peritonitis, and hepatorenal syndrome, however, its long-term use is controversial. The objective of this review was to identify if the prolonged use of albumin has beneficial effects in the treatment of cirrhotic patients. Methodology. PubMed database was searched using the following terms: ("Liver Cirrhosis"[Mesh]) AND ("Serum Albumin"[Mesh] OR "Serum Albumin, Human"[Mesh]). Articles that did not meet the topic and those that were more than 5 years old were excluded, except for those relevant to the review. Results.It has been shown in several studies within the previous 4 years, that prolonged administration of albumin reduces mortality in cirrhotic patients. In addition, it results in a decrease in hospital ad-missions due to complications of cirrhosis, a decrease in the need for paracentesis and less use of albumin for other established indications, which offsets the costs derived from therapy. Conclusion. It is concluded based on the evidence presented, that the long-term use of albumin could be beneficial in patients with decompensated liver cirrhosis. However, other aspects of the therapy need to be addressed in further studies

Emodin inhibits bladder inflammation and fibrosis in mice with interstitial cystitis by regulating JMJD3

Purpose: Interstitial cystitis/bladder pain syndrome (IC/BPS) is a devastating urological chronic pelvic pain condition. In search of a potential treatment, we investigated the effect of emodin on IC/BPS inflammation and fibrosis, and explore the potential mechanism. Methods: An experimental model of interstitial cystitis was induced by cyclophosphamide, and human bladder smooth muscle cells were treated with lipopolysaccharide to establish the cell model in vitro. In both models, inflammation- and fibrosis-related indexes were measured after emodin administration. Furthermore, the specific antagonists were used to dig for the mechanisms underlying the response to emodin treatment. Results: Emodin significantly ameliorated management of cystitis, reduced the amount of inflammatory cytokines (tumor necrosis factor-α, monocyte chemoattractant protein-1, interleukin-1ß, interleukin-8, and interleukin-6) in models, as well as reducing the synthesis of fibrosis marker including collagen1, collagen3, vimentin, fibronectin and α-smooth muscle actin. Further mechanism studies demonstrated that emodin inhibited inflammatory reaction and fibrosis through blocking lysine-specific demethylase 6B (JMJD3) expression via JAK/STAT, NF-κB and TGF-ß/SMAD pathways. Conclusions: Our study reveals the critical role of emodin-JMJD3 signaling in interstitial cystitis by regulating inflammation, fibrosis, and extracellular matrix deposition in cells and tissues, and these findings provide an avenue for effective treatment of patients with cystitis.

Diagnóstico clínico, radiográfico e histológico de un caso de fibrosis periapical posendodóntica / Clinical, radiographic, and histologic diagnosis of a postendodontic periapical fibrosis case

Objetivo: La fibrosis periapical posendodóntica es un proceso reparativo asintomático, radiolúcido y no progresivo que se interpreta con frecuencia como una lesión patológica persistente. El diagnóstico de esta entidad suele ser dudoso y sólo puede definirse mediante la correlación de las obser- vaciones clínicas, radiográficas e histológicas. El objetivo de este informe es describir el caso de un paciente que presenta un área radiolúcida periapical persistente y asintomática en un incisivo lateral superior. Caso clínico: Luego de cuatro años y dos meses de ha- ber recibido un tratamiento endodóntico el paciente concurre a la consulta para un examen de rutina. El examen radiográfico del diente revela un área radiolúcida persistente y bien defini- da. A causa de una fractura radicular irreparable, se indicó la extracción de la pieza dentaria. Esto permitió realizar el estu- dio histológico del tejido blando que permanecía adherido en el ápice de la raíz, lo que confirmó y completó el diagnóstico de fibrosis periapical posendodóntica.(AU)

Aim: The postendodontic periapical fibrosis is an asymp- tomatic radiolucent and non-progressive healing process that is often interpreted as a persistent pathological lesion. The diagnosis of this entity is usually uncertain, and it is only de- fined by the correlation of clinical, radiographic and histo- logical observations.The aim of this report is to describe the case of a patient with a long-term persisting asymptomatic and radiolucent area in a upper lateral incisor. Clinical case: Four years and two months after receiv- ing an endodontic treatment the patient comes to our office for a routine control. Radiographic examination revealed the presence of a persistent well defined radiolucent area. Sur- gical tooth extraction was required due to the presence of a complicated root fracture.This allowed to perform a histolog- ical study of the soft tissue attached to the apex of the ex- tracted root, which confirmed and completed the diagnosis of postendodontic periapical fibrosis (AU)

Frequência de esteato-hepatite alcoólica em pacientes portadores do vírus de hepatite C / Frequency of alcoholic steatohepatitis in patients with hepatitis C virus

Introdução: o consumo de álcool é um fator de risco bem conhecido para induzir doença crônica do fígado. O álcool também é um cofator na patogênese induzida pelo vírus da hepatite C (VHC). A infecção crônica pelo VHC pode exacerbar a lesão hepática alcoólica por mecanismos que incluem aumento do estresse oxidativo. Portanto o VHC, concomitantemente com o consumo excessivo de álcool, induz diversos mecanismos fisiopatogênicos que contribuem para a diminuição da depuração viral e para a lesão hepática. Objetivos: 1 ­ avaliar a frequência de esteato-hepatite alcoólica em biópsias de pacientes portadores do vírus da hepatite C; 2 ­ estudar os estágios da fibrose hepática nesses pacientes versus pacientes com e sem ingestão de álcool; 3 ­ analisar os escores bioquímicos e antropométricos desses pacientes. Metodologia: estudo de corte transversal, com pacientes acompanhados no núcleo de hepatologia do Hospital Prof. Edgard Santos da Universidade Federal da Bahia, portadores de hepatite C, com laudos de biópsias disponíveis para avaliar presença de esteato-hepatite alcoólica comprovada pelo registro de consumo de gramas de álcool. Foram considerados etilistas homens que consumiam mais de 30 g por dia e mulheres com consumo maior do que 20 g por dia. As variáveis utilizadas basearam-se em critérios histológicos, epidemiológicos e clínicos aplicados a esses pacientes. Resultados: a amostra total de pacientes portadores de hepatite C analisados foi de 335, sendo 100 indivíduos considerados com ingestão elevada de álcool, e 28,9% dos casos da amostra. A presença de esteatose hepática sem esteato-hepatite foi em 34 indivíduos (10,15%), e os casos de esteato-hepatite aparecem em um total de 30 indivíduos (8,96%). A carga viral elevada dos pacientes, tendo como referência >800.000, esteve em n=102, com 30,4% dos casos de VHC. Conclusão: observou-se, na população de estudo, 43 % os portadores de VHC com uso excessivo de alcool, 8,9 6% tinham esteato-hepatiits e 10,15 % esteatose. Além disso, verificou-se que mais da metade desses pacientes (56,6%) apresentaram grau de fibrose moderada e 53,3%, atividade necroinflamatória leve. A comorbidade mais comum observada foi hipertensão arterial sistêmica (HAS), em 40% dos pacientes.

Introduction: alcohol consumption is a well-known risk factor for inducing chronic liver disease, alcohol is also a cofactor in the pathogenesis induced by Hepatitis C Virus (HCV). Chronic HCV infection can exacerbate alcoholic liver damage by mechanisms including increased oxidative stress. Therefore, HCV, concomitantly with excessive alcohol consumption, induces several pathophysiological mechanisms, which contribute to the decrease in viral clearance and liver damage. Objectives: 1 ­ to assess the frequency of alcoholic steatohepatitis in biopsies of patients with the hepatitis C virus, 2 ­ to study the stages of liver fibrosis in these patients versus in patients with or without alcohol intake, 3 ­ analyze biochemical and anthropometric scores of these patients. Methodology: cross-sectional study, with patients monitored at the hepatology center of Hospital Prof. Edgard Santos from the Federal University of Bahia, carriers of hepatitis C with biopsy reports available to assess the presence of alcoholic steatohepatitis proven by recording the consumption of grams of alcohol, considered an alcoholic being a man, who consumed more than 30 g per day and being woman more than 20g a day. The variables used were based on histological, epidemiological and clinical criteria applied to these patients. Results: the total sample of patients with hepatitis C analyzed was (n=335), with n=100 individuals considered to have high alcohol intake, and 28.9% of the cases in the sample. The presence of hepatic steatosis without steatohepatitis was in 34 individuals (10.15%), and cases of steatohepatitis appear in a total of n=30 individuals (8.96%).The high viral load of patients, with >800,000 as reference, was n=102, with 30.4% of cases of HCV. Conclusion: it was observed, in the study population, 43% of HCV carriers with excessive alcohol use, 8.96% had steatohepatitis and 10.15% steatosis. Furthermore, it was found that more than half of these patients (56.6%) had a moderate degree of fibrosis and 53.3% had mild necroinflammatory activity. The most common comorbidity observed was systemic arterial hypertension (SAH), in 40% of patients.

Autoimmune myelofibrosis and systemic lupus erythematosus: a case report

Bone marrow fibrosis is a rare disorder that can be associated with autoimmune diseases such as systemic lupus erythematosus (SLE), and can be confused with the manifestations of that disease. The case is presented on a patient with autoimmune myelofibrosis in the context of SLE.

La fibrosis de la médula ósea es una enfermedad rara que se puede ver asociada con enfermedades autoinmunes como el lupus eritematoso sistémico (LES) y que puede llegar a ser confundida con las manifestaciones propias de la enfermedad. Se presenta el caso de una paciente con mielofibrosis autoinmune en el contexto de LES.

The behavior of liver diseases in a cohort of Colombian patients with COVID-19 / Comportamiento de las enfermedades hepáticas en una cohorte de pacientes colombianos con COVID-19

Abstract Introduction: Severe acute respiratory syndrome type 2 coronavirus infection (SARS-CoV-2) is receiving the most attention now. The asymptomatic elevation of transaminases is typical in the liver, and liver involvement varies from 14 % to 78 %. The assessment of liver comorbidities is scarce, with prevalence ranging between 2 % and 11 %. Aim: To describe the behavior of a cohort of patients with liver diseases who fell ill with coronavirus disease 2019 (COVID-19). Materials and methods: This retrospective observational study analyzed the behavior of a cohort of patients with liver diseases who fell ill with COVID-19. Results: 543 patients became ill with COVID-19, of which 300 were women (55.3 %). The median age at diagnosis of liver disease was 52 years. The leading causes of liver disease were nonalcoholic steatohepatitis (49.5 %), cholestatic disease (7.7 %), and hepatitis C and B viruses (6.3 %). Alanine aminotransferase (ALT) had a median of 52 U/L (interquartile range [IQR]: 30-98) and aspartate aminotransferase (AST) 32 U/L (IQR: 23-62). Mortality due to viral infection was 5.7 %, with an incidence rate of 2.9 (95 % confidence interval [CI]: 2-4.2). Conclusions: It is a retrospective study but, until the preparation of the manuscript, it had been the first cohort in Colombia to describe the behavior of liver diseases in patients who become ill with COVID-19. No statistically significant differences were found between the causes of liver disease that confer a higher risk of mortality; however, having decompensated cirrhosis is the only condition related to mortality.

Resumen Introducción: la infección por coronavirus del síndrome respiratorio agudo grave de tipo 2 (SARS-CoV-2) concentra la mayor atención en el momento. En el hígado es frecuente la elevación asintomática de transaminasas y la afectación hepática varía del 14 % al 78 %. La evaluación de las comorbilidades hepáticas es escasa, con prevalencias que oscilan entre el 2 % y el 11 %. Objetivo: describir el comportamiento de una cohorte de pacientes con enfermedades hepáticas que presentaron el coronavirus de 2019 (COVID-19). Materiales y métodos: estudio observacional retrospectivo que analizó el comportamiento de una cohorte de pacientes con hepatopatías que enfermaron por COVID-19. Resultados: 543 pacientes padecieron por COVID-19, de los cuales 300 fueron mujeres (55,3 %). La mediana de edad al diagnóstico de la enfermedad hepática fue de 52 años. Las principales causas de las hepatopatías fueron esteatohepatitis no alcohólica (49,5 %), enfermedad colestásica (7,7 %), virus de la hepatitis C y B (6,3 %). La alanina-aminotransferasa (ALT) presentó una mediana de 52 U/L (rango intercuartílico [RIC]: 30-98) y aspartato-aminotransferasa (AST) 32 U/L (RIC: 23-62). La mortalidad por la infección viral fue del 5,7 % con una tasa de incidencia de 2,9 (intervalo de confianza [IC] 95 %: 2-4,2). Conclusiones: es un estudio de carácter retrospectivo; sin embargo, hasta la elaboración del manuscrito es la primera cohorte en Colombia en describir el comportamiento de las enfermedades hepáticas en pacientes que enferman de COVID-19. No se encontraron diferencias estadísticamente significativas entre las causas de hepatopatía que confieran un mayor riesgo de mortalidad; sin embargo, tener una descompensación de cirrosis es la única condición que tiene una relación con la mortalidad.

Fibrosis congénita de los músculos extraoculares / Congenital Fibrosis of Extraocular Muscles

La fibrosis congénita de los músculos extraoculares se caracteriza por una oftalmoplejía externa congénita, no progresiva, generalmente bilateral, con ptosis y alteración de los movimientos oculares. Existen varios tipos en dependencia del gen afectado y puede estar acompañada de hallazgos adicionales tanto oculares como generales. Para el manejo de los casos se realiza cirugía de la ptosis, alineación ocular y corrección del torticolis, además de su corrección óptica y rehabilitación para maximizar el resultado visual. Con el objetivo de estar al día sobre esta enfermedad se realiza una revisión de las publicaciones de los últimos cinco años en este tema. Actualmente no hay tratamientos que puedan restaurar la funcionalidad completa y el rango de movimiento de los músculos extraoculares, pero mejorar su funcionalidad visual es primordial(AU)

Congenital fibrosis of the extraocular muscles is characterized by congenital external ophthalmoplegia, nonprogressive, usually bilateral, with ptosis and altered eye movements. There are several types depending on the affected gene and it may be accompanied by additional ocular or general findings. For the management of these cases, ptosis surgery, ocular alignment and torticollis correction are performed, as well as optical correction and rehabilitation to maximize visual outcome. In order to be updated about this disease, a review of the publications on this subject within the last five years is carried out. Currently, there are no treatments that can restore full functionality and range of motion of the extraocular muscles, but improving their visual functionality is paramount(AU)